Host-Microbe Relationship Flashcards
1
Q
How are we composed of microbes?
A
- our own bodies are only 1/2 our own (recent study found that we have resident bacterial community w/ an approximately equal number of cells to our own)
- our genomes contain a stunning number of ancient, endogenous, retroviruses (estimated to account for 5-8% of our genetic material!)
2
Q
What important functions do microbes perform?
A
- lack to nitrogen fixing bacteria (decreased plant growth)
- w/o oxygenic microorganisms (increased atmospheric CO2)
- no microbes to break down waste (accumulating ‘waste’ biomass)
- some microbes are delicious
3
Q
What are Koch’s postulates?
A
- microoganism must be found in abundance in all organisms suffering from disease, but should not be found in healthy organisms
- microorganisms must be isolated from a diseased organism & grown in pure culture
- cultured microorganism should cause disease when introduced into a healthy organism
- microorganism must be reisolated from the inoculated, diseased experimental host & identified as being identical to the original specific causative agent
4
Q
How are Koch’s postulates related to real pathogens?
A
- strictly speaking, very few organisms act as “pathogens” as defined by Koch’s postulates (most are between obligate pathogens and non-pathogenic colonizers; ex: e-coli 0157 is a potentially serious human pathogen, but bovine commensal)
- there are very few strict pathogens (rabies - although maybe not in bats?; Yersinia pestis (plague) in people & domestic animals)
5
Q
What is a pathogen?
A
organism capable of causing disease
6
Q
virulence
A
relative ability of an organism to cause disease
7
Q
virulence factor
A
property of an organism which allows it to establish w/in a host and/or cause disease
8
Q
what is pathogenesis?
A
processes & host-organism interactions which lead to disease
9
Q
What is the spectrum of host-microbe interactions from the host’s perspective?
A
- benefit (colonization w/ normal microbiota)
- indifference (latency)
- damage (disease)
10
Q
When does disease happen?
A
- infections occur when (there is an overwhelming pathogen load and/or compromised host defenses)
- disease/pathology/damage results from (production of toxins and/or the invasion of tissues)
11
Q
What are the fundamentals of pathogenesis?
A
- associate (enter body or reach site of infection: anatomical location, cell type, or receptor)
- multiply & evade (acquire & utilize nutrients, multiply & reach critical number while avoiding/countering host defenses)
- damage/co-opt (damage from pathogen, or host response +/- hijacking host processes. toxins, using host machinery for invasion, etc.)
- transmit (get out, survive, infect, repeat! efficiently shed infectious organism)
NOT A LINEAR PROCESS!
12
Q
What are the overarching types of virulence factors?
A
- essential virulence genes (those which cause demonstrable damage to host)
- virulence associated genes (required for expression, secretion, or processing VF)
- virulence lifestyle genes (allow organism to colonize host or reach site of infection)
13
Q
List of virulence factors:
A
- structures used for attachment
- flagella
- siderophores
- capsule
- secretion systems
- toxins
- superantigens
- enzymes
14
Q
What are examples of structures used for attachment?
A
- Staphs & Streps - Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs): proteins which bind to host ligands (fibrinogen, collagen, fibronectin, etc.); MSCRAMMs may also be anti-phagocytic by preventing opsonization)
- fimbriae: F4 fimbriae in E. coli - bind to intestinal epithelium in piglets up to ~8wk old; F5 fimbriae in E. coli - bind to epithelium in distal sm intestine in calves ~ first few days old
15
Q
What are flagella used for?
A
reaching the site of infection
- motile E. coli swimming up ureters to cause ascending pyelonephritis following a lower UTI
- Brachyspira spp. moving through colonic mucous to reach intestinal crypt
16
Q
what are siderophores?
A
- free iron is a limiting nutrient even in blood - its VERY tightly bound!
- these chelators allow bacteria to capture iron in a very low concentrated environment (Enterobactin, Yersiniabactin, Pyoverdin, Pyocyanin)
17
Q
What is a capsule?
A
- polysaccharide struct
- interferes w/ innate immune system (prevents phagocytosis & attachment of complement)
- can also protect from bacteriophages!
18
Q
What are the secretion systems?
A
- structures which transport molecules across the cell envelope
- type 3 secretion system of Salmonells is used to inject effector molecules into the host cells (needle like apparatus)
19
Q
What are bacterial toxins?
A
wide variety of actions on target receptors / cells / tissues : endotoxin - lipopolysaccharide (LPS); exotoxin - (ex: botulinum toxin, shiga toxin, cholera toxin)
20
Q
What are superantigens?
A
antigens which are able to non-specifically bind to & activate T-cell receptor, resulting in “cytokine storm”
21
Q
What are the degrees of pathogenicity and what affects them?
A
- pathogenicity is non-binary
- can be accidental pathogen, opportunist facultative, or obligate pathogen
- is the organism pathogenic? is the host susceptible to infection? is the environment permissive to infection?
22
Q
What is the damage-response framework?
A
23
Q
What are some examples of saprophytes or environmental pathogens?
A
- Rhodococcus equi: cause of pneumonia in foals; otherwise healthy animals ~12 wks old; probably due to decline in maternal immunity; also seen in transplant, cancer, & AIDS patients
- Aspergillus: ubiquitous in nature; decomposing matter; cause of pneumonia & air sacculitis in birds; allergic airway disease in horses)
24
Q
What are opportunistic pathogens?
A
- most clinically relevant organisms are probably best described as somewhere in the opportunistic spectrum
- gaining access to normally sterile site = infection (Staphylococcus spp.: mastitis, UTI, surgical site infections; Dermatophilus congolensis: cause of rain scald - occurs when wet, macerated skin is traumatized; E. coli: bacteremia/sepsis in most spp, UTI)
25
Difference btwn primary and secondary infections?
- is your patient's infection secondary to a larger problem?
- determine WHY your patient has an infection, & then dealing with the underlying problem is critical!
- ex: is the disease in a dog (UTI) resulting from another disease? (UTI in dog secondary to diabetes, ectopic ureters, bladder cancer?)
- is the disease resulting from poor management? (failure to clean milking equipment leading to mastitis; overcrowding of pigs & failure to dock tails leading to tail biting & ascending infections of the spinal cord)
26
What are the three components of the epidemiological triad?
1. favourable environment
2. virulent agent
3. susceptible host
27
What influences a favourable environment?
- agent & host are in same environment
- favourable conditions (ex: flooding vs drought)
- presence of vectors/reservoirs
- change that facilitates spread
- change that alters host susceptibility
28
What influences a virulent agent?
- possession of requisite virulence factors
- sufficient numbers
- change in virulence?
29
What influences a susceptible host?
- herd immunity
- individual susceptibility
- nutrition
- co-morbidities
- age
30
What is an example of the epidemiological triad at work?
Earthquake in Haiti
- host: > 1 million displaced people; cholera-negative, naiive population
- agent: vibrio cholerae - waterborne disease; tragically brought to Haiti by aid workers
- environment: devasted infrastructure in already desperately poor country; lack of adequate water sanitary systems (both sewage & drinking water)
31
What is a zoonoses?
- infectious disease caused by pathogen that has jumped from a non-human animal to a human
- typically, 1st infected human transmits infectious agent to @ least 1 other human, who, in turn, infects others
- in contrast, transmission can also occur via intermediate sp (vector), which carry disease pathogen w/o getting sick
- when humans infect other animals, it's called reverse zoonosis
32
What should we think about in terms of interspecies transmission?
- why privilege discussions of interspecies transmission to a human perspective? (zoonoses, reverse zoonoses)
- what about transmission btwn different animals?
- think of transmission from the organism's perspective
- tendency to classify as "zoonotic" or not is too reductive
33
BIG PIC: What are Koch's postulates? Describe a situation where the postulates fall short?
1. microoganism must be found in abundance in all organisms suffering from disease, but should not be found in healthy organisms
2. microorganisms must be isolated from a diseased organism & grown in pure culture
3. cultured microorganism should cause disease when introduced into a healthy organism
4. microorganism must be reisolated from the inoculated, diseased experimental host & identified as being identical to the original specific causative agent
- strictly speaking, very few organisms act as "pathogens" as defined by Koch's postulates (most are between obligate pathogens and non-pathogenic colonizers; ex: e-coli 0157 is a potentially serious human pathogen, but bovine commensal)
- there are very few strict pathogens
34
BIG PIC: What are 3 components of the epidemiological triad?
- susceptible host
- virulent agent
- favourable environment
